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BDE-47 会破坏发育中的斑马鱼的轴突生长和运动行为。

BDE-47 disrupts axonal growth and motor behavior in developing zebrafish.

机构信息

Zhejiang Provincial Key Laboratory for Technology and Application of Model Organisms, Institute of Watershed Science and Environmental Ecology, Wenzhou Medical College, Wenzhou 325035, China.

出版信息

Aquat Toxicol. 2012 Sep 15;120-121:35-44. doi: 10.1016/j.aquatox.2012.04.014. Epub 2012 Apr 28.

DOI:10.1016/j.aquatox.2012.04.014
PMID:22609740
Abstract

Polybrominated diphenyl ethers (PBDEs) are ubiquitous environmental pollutants detected in a wide variety of environmental matrixes and pose a significant public health concern. 2,2',4,4'-Tetrabromodiphenyl ether (BDE-47) is one of the most predominant PBDE congeners in environmental media, biota and human tissues. However, few studies have explored the BDE-47 developmental neurotoxicity and underlying mechanisms. In this study, zebrafish (Danio rerio) embryos were waterborne exposed to BDE-47 at 1.25, 5, 20 μM starting from 6h post-fertilization (hpf). Motor behavior development and swimming behavior in response to light-to-dark photoperiod stimulation were studied at various developmental stages. Our data indicate that BDE-47 exposure significantly affected spontaneous movement, decreased touch response and free swimming speed, altered larvae swimming behavior in response to light stimulation in developing zebrafish. Consistent with these motor deficits, BDE-47 significantly inhibited axonal growth of primary and secondary motor neurons during the early developmental stages, suggesting the functional relevance of structural changes. Our findings demonstrate that the altered patterns of neuronal connectivity may contribute to motor behavior deficits, indicating the relevance of zebrafish as a model for studying toxicant developmental neurotoxicity.

摘要

多溴联苯醚(PBDEs)是广泛存在于各种环境基质中的环境污染物,对公共健康构成了重大威胁。2,2',4,4'-四溴二苯醚(BDE-47)是环境介质、生物群和人体组织中最主要的多溴联苯醚同系物之一。然而,目前很少有研究探讨 BDE-47 的发育神经毒性及其潜在机制。在这项研究中,斑马鱼(Danio rerio)胚胎从受精后 6 小时(hpf)开始,通过水暴露于 1.25、5、20 μM 的 BDE-47 中。在不同的发育阶段研究了运动行为发育和对光暗光周期刺激的游泳行为。我们的数据表明,BDE-47 暴露显著影响自发运动,降低了触觉反应和自由游泳速度,改变了发育中的斑马鱼对光刺激的幼虫游泳行为。与这些运动缺陷一致,BDE-47 在早期发育阶段显著抑制了初级和次级运动神经元的轴突生长,表明结构变化的功能相关性。我们的研究结果表明,神经元连接模式的改变可能导致运动行为缺陷,表明斑马鱼作为研究毒物发育神经毒性的模型的相关性。

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